Resp Flashcards
Lung function tests
Obstructive vs restrictive lung disease
Examples for each (3-4)
Obstructive = FEV1:FVC <75%
asthma, COPD.
Restrictive = FEV1: FVC >75%
interstitial lung disease, rib #, MSK - chest deformity/scoliosis, neuro (MND), obesity
COPD
- diagnosed based on clinical presentation + spirometry finding:
- How to asseess for impact of breathlessness?
- severity scale, using FEV1 % of predicted…
- potential genetic underlying cause.
- what can it lead to?
- TLCO?
- All FEV1:FVC <0.7. Severity characterised by the FEV1: >80%, 50%, 30%, <30%
Obstructive picture without dramatic response to reversibility testing. - MRS Dyspnoea scale - Grade 1 - 5 (mild; SoB with strenuous exercise to 5 - house bound).
- Severity: 1-4; FEV1 >80, 70, 50, 30% of predicted.
- A-1 antitrypsin deficency - COPD & CLD.
- Polycythaemia.
- Transfer factor for CO is decreased in COPD.
Long-term mx for COPD
- First line treatment options (2)
Second line depends on whether COPD is steroid responsive/pt has asthmatic features
- Mx if YES; Mx if NO.
- 3rd line mx.
- Additional drugs include (3).
- Bronchodilator therapy (SABA- Salbutatmol, or SAMA - Ipatropium bromide)
- Combination therapy:
if steroid responsive –> LABA + ICS (e.g. Salmeterol + Beclometasone). Keep short acting: SAMA or SABA.
If NOT steroid responsive–> LABA + LAMA (e.g. Tiotropium)
- keep shortacting therapy (SABA only).
- Combination therapy:
- Triple therapy for steroid responsive: LABA + LAMA + ICS (e.g. *Salmeterol + Tiotropium + Beclometasone).
Additionals - oral theophylline, mucolytics (Carbocysteine), abx prophylaxis w Azithromycin
akaif steroid responsive there are more options: you can use steroids an
Mx COPD Exacerbation
1. At home
2. In hospital - admit if severe SOB, confusion/low GCS, cyanosis, <90% O2, social reasons, significant comorbidity
3. If severe; not responding to 1st line
4. Not responding to 1st line/ ABG shows resp acidos - what type of NIV is preferred?
5. Further management
Oxygen therapy
* mask of choice
* target sats before/after ABG
What is Doxapram?
- Pred (30mg OD 5/7)
increase freq of bronchodilartor via inhaler/nebs
antibiotics - Amoxicillin or Clarithromycin (if infective exacerbation - purulent sputum & other signs) - Nebs bronchodilator therapy (SABA/SAMA)
systemic steroids (IV hydrocortisone or oral pred)
Abx (if infective)
chest physio. - If not responsding to neb bronchodilator –> IV Amniophylline –> NIV
- NIV = BiPAP (better for acid-base balance and preventing inhaling exhaled gases)
- Intubation and ventilation/HDU admission
Oxygen
Venturi mask 28% at 4l/min
Assume 88-92% sats (Co2 retainer)
If pCO2 normal on ABG: adjust to 94-98%
A resp stimulant if NIV/intubation not appt.
LTOT:
2 x ABGs with a pO2 of what is an indication for at home oxygen therapy for COPD?
Or between X and X with secondary causes/RFs (4)
<7.3
or 7.3-8 with:
secondary polycythaemia
pulmonary htn
peripheral oedema
cannot be used if smoke
pO2 <7.3 kPA or between 7.3 and 8 with the secondary features
Asthma
* specific sx suggestive of diagnosis
* examination findings
* BTS - can make a diagnosis clinically. NICE advise using a diagnostic hub. What are the first line inv advised by NICE (2)
* Further testing options (2)
* Diagnostic criteria - 2 (post-bronchodilator improvement in FEV1 and of lung volume) and exhaled FENO
- SoB, wheeze, cough, chest tightness - episodic sx with diurnal variability
- widespread polyphonic wheeze
1. Spirometry w bronchodilator reversibility
2. FeNo - Note a neg spirometry test doesn’t rule out asthma.
- Peak flow variability (diary of PEFR several times a day 4 weeks) & direct bronchial challenge test (histamine/methacholine)
Diagnostics
Post bronchodilator therapy:
>200ml lung volume
12% or greater FEV1
Or exhaled FeNO >40p/billion
Asthma mx - adults
- 4 main steps (add on drugs)
- further steps (increasing dose, or using alternatives)
How does this differ from management of asthma in children (5-16)?
And for children under 5?
- SABA
- +low doseICS(Beclometasone inh)
- +LTRA(Montelukast)
- +LABA
- +MART- ICS + SABA -combination therapy in one inhaler (+/- LTRA)- instead of individuals
Further steps
- Increase ICS dose low –> medium
- Try theophylline or LAMA
- Seek expert advice
In paeds; NICE recommend stopping the LTRA when trying out the MART. And the ICS used are “paediatric low dose”.
Children under 5:
1. start on a SABA
2. 8-week trial of a paed moderate-dose ICS - if did not resolve, ? other diagnosis. If resolved - restart moderate dose ICS as maintenance. if resolve but reoccured - repeat trial.
3. SABA + paed low dose ICS + LTRA
4. Stop LTRA and seek expert advice
Acute asthma exacerbation:
PEFR, speech, RR, O2, CO2, signs of shock
Moderate
Severe
Life-threatening
Near fatal
Moderate
PEFR 50-75% predicted
Speech normal
RR<25 and PR <110
Severe
PEFR 33-50%
Unable to complete sentences
RR >25 and RR >110
Life-threatening
PEFR <33%
SpO2 <92%
Silent chest, cyanosis, reduced resp effort.
Normal CO2 - reduced resp effort.
Hypotension; bradycardia
Exhaustion, confusion; coma.
Near fatal
Raised PaCO2 +/- requiring mechanical ventilation with raised inflation pressures (doesn’t use PEFR as a feature)
Mx for acute asthma exacerbation
General
Moderate
Severe
Life-threatening
Near-fatal
General
* A-E(O2 if sats low); ABG
Moderate
* SABA inh/oxygen-driven nebs/PMDI
* + SAMA
(SalbutamolAND Ipatropium bromide)
* + Prednisolone PO or Hydrocortisone IV
Severe
* + IV MgSo4
Life-threatening
* + Aminophylline/IV Salbutamol
* Admission to HDU/ICU –> intubation in worst case/ECMO
Near-fatal
Req Mechanical ventilation
when on salbutamol what must be monitored
serum K+ (salbutamol can cause hypokalaemia)
and note salbutamol induced tachycardia
Bronchiecstasis key points
-definition
- how many weeks of recurrent infections?
- presentation (4)
- findings (CXR and HRCT)
- mx (conservative)
A condition of airways obstruction caused by long-term inflammation from recurrent infections >8 weeks –> lung fibrosis. Presents with long hx of cough with thick sputum +/- haemoptysis, SoB and fever in exacerbations. Diagnosed on CXR (bronchial dilation) and to assess extent of disease on HRCT (tramlines & rings, pools of mucus). Conserv trt for chronic disease- mucolytics, chest physio, smoking cessation.
Features specific to underlying micro-organism causing pneumonia
Typical
Gram +ve
1. Strep p.
2. Staph aures
Gram -ve
2. Haemophilius influenzae
3. Klebsiella
4. Moxarella catarrhalis
5. psuedomonas aureginosa
Atypicals - cannot be identified by gram stain or treated with penicillins
1. Mycoplasma p.
2. Legionella
3. Coxiella burnetti
4. pstiacci
Viral
* influenza A&B
* varicella zoster & herpes simplex
* SARS/COVID-19
Fungal - if immunocompromised
- Pneumocystis jirovecci (PCP)
Typicals
* * Most frequent, rusty sputum, associated with herpes labialis
* common in elderly, or secondary to influenza, and CF
* most common in COPD/existing lung disease - may produced beta-lactamase (abx resistant)
* alcoholics/diabetics; red current jelly sputum, increasing resistance, upper lobe consolidation
* immunocompromised/chronic lung disease
* CF/bronchiecstasis
Atypicals: legions of pstiacci MCQs
1. epidemics; has autoimmune features e.g. erythema multiforme/erythema nodosum rash and cold AIH; GBS or immune-mediated neurolgoical diseases Affects younger patients. Prolonged/gradual onset. Requires mycoplasma serology and agglutination test. Requires Doxy or macrolide.
2. travel related from infected water –> legionnairre’s disease (abdo pain, diarrhoea, mental state cx) - requires urinary antigen testt by urne sample. Hyponatraemia.
3. zoonose - can cause Q fever and infective endocarditis.
Fungal
- HIV associated; req. Septic (Cotrimoxazole)
Severity assessment as a predictor of mortality- pneumonia.
Score 0/1 -
>2 -
»3 -
C(U)RB-65 =
* Confusion, AMTSS <=8
* Urea >7
* RR >30
* BP <90/60
* >65
*
0/1 - consider tx at home
>=2 - hospital admission
>=3 - ITU
Tuberculosis infectious disease caused by mycobacterium tb , an acid fast bacteria staining red with Zeil-Neelsen stain
* stages of disease
* vaccination - contents and preliminary step
* who is offered BCG?
* extra-pulmonary TB (3)- bones, skin, lymph nodes?
* Ix - CXR, sputum cultures and 2 special tests
- active, latent, reactivated, milary (disseminated)
- BCG- live TB, requires Mantoux -ve.
- Neonates born in areas or with FHx of high rates of TB. Older children/adults who recently arrived in country with high rates or who are in cloe contact. Healthcare workers.
- Pott’s disease (TB of the spine); erythema nodosum, lymphadenopathy.
- Mantoux test (+ve in previous, active or latent TB).
- IGRA:interferon gamma release assay (+ve if latent TB - aka no sx and -ve mantoux).
Chest xray findings for TB
- primary
- reactivated
- disseminated
- patchy consolidation, pleural effusions, lymphadenopathy
- nodular consoliation & cavities
- millet seeds
TB medications and side effects
- Rifampicin (orange bodily fluids)
- Isoniazid (peripheral neuropathy)
- Pyrazinamide (hepatoxicity; high uric acid - gout (toe on fire)
- Ethambutol (retinopathy - visual acuity & colour blindness)
Other mx considerations for TB
- PHE notification
- Testing for Hep B and Hep C
- Isolation 2 weeks in negative pressure rooms
- Mx by MDT - esp. extrapulmonary e.g. steroids
- individualised drug regime for MDRTB
Drug induced pulmonary fibrosis (fibrOsis) (4)
- MethOtrexate
- AmiOdarone
- NitrOfurantoin
- CyclOphosphamide
Nitro, cyclo, metho, amio
Acute resp
Pulmonary embolism
* Px
* Risk factors
* Ix
* Wells score takes into account (3)
* How else can a definitive diagnosis be made?
* Mx: stable patients (1st line, 2ndline - c/i)
* Mx: unstable “massive PE” - aka hypotension
* Length of anticoagulation : provoked/unprovoked
- sudden onset chest pain, worse on inspiration with SoB
- O/E - reduced lun sounds and air entry on affected side
- VTE - immobility, blood stasis, anti-phospholipid syndrome
- A-E, O2, CXR, ABG>
- Wells score -pmhx, clinical signs, malignancy- Tachcardia, recent surgery, haemopytis etc - if >2 - PE likely –> CTPA. If <2 - D-dimer to exclude it (unless +ve –> CTPA).
- V-Q scan
PE Management
* 1st line - Anticoagulation: DOACs (apixaban/rivaroxaban) if diagnosis is suspected; includes cancer pts
* 2ndline if DOACs contra-indicated; eGFR <15, APLS aka triple negative - LMWH then Warfarin
* Massive PE: thrombolysis with alteplase
Length of anticoagulation
* provoked: 3 months
* provoked, active cancer: 3-6mo
* unprovoked: 6 months
Spontaneous Pneumothorax
* Define
* Px, O/E
* Risk factors
* Erect CXR findings (–>CT thorax if small)
- air trapped within the pleural space; “collapsed lung”
- sudden onset chest pain, SoB
- O/E - hyperresonant on affected side. Tracheal deviation (towards affected side)
- Spontaneous - Tall, thin males, athletic. Or secondary to other condition.
- CXR - loss of lung markings, visible edge of lung
Spontaneous pneumothorax management: decision algorithm
* No/minimal symptoms?
* List the 6 high risk characteristics
* Symptomatic with H-R C
* Symptomatic WITHOUT H-R C
Which pneumothoraces are deemed safe to intervene, and how?
Explain the management for conservative care and ambulatory care.
High-risk characteristics
1. Haemodynamic compromise (?tension)
2. Significant hypoxia
3. Bilateral
4. Underlying lung disease
5. >=50 with sig smoking hx
6. haemothorax
Treatment algorithm
- No/minimal sx -> conservative
- Not high risk–> conservative, ambulatory device or needle aspiration
- High risk & safe to intervene –> chest drain
Safe to intervene - pneumothorax is 2cm or can be safely accessed with radiological support
Conservative
- primary: OP review 2-4days
- secondary: IP then OP f/up
Ambulatory
- Rocket Pleural Vent - one way valve
Needle aspiration
- once resolved requires discharge and OP f/up
Massive PE
- Definition
- Mx (first-line)
- Recurrent PE mx
PE with haemodynamic instability; e.g. saddle PE
Throbolysis
Or other invasive approaches
IVC filters (stop DVT formation)
Tension (traumatic) pneumothorax
* define
* e.g. caused by
* examination findings
* emergency mx –> definitive
- trauma/subclavian centril line insertion
- air within the pleural space that forms a one-way valve; allowing air in but not air out –> pressure and haemodynamic compromise
- O-E - resonant to percussion; increased air entry on affected side, tracheal deviation away from affected side; haemodynamic instability
- A-E; relieve pressure -emegency arge bore cannula into the 2nd ICC mid clavicular line
- Chest drain into triangle of safety - 5th ICC - vertical line (nipple) horizontal - anterior & middle axillary lines. CXR to ensure positioning away from neurovascular bundle.
Pleural effusion
Collection of fluid within the pleura; presenting with pleuritic chest pain, SoB and cough.
* O/E
* Difference between transudative and exudative?
* Bloods (FBC, U&E, LFT, amylase); CXR (AP) and pleural fluid sample (protein, LDH, pH, microbiology & cytology)
* CXR findings
* Explain Light’s criteria for diagnosis of exudative effusion
*
- Dull to percussion; reduced air entry, reduced breath sounds, decreased tactile fremitus, tracheal deviation to opposite side (if massive)
- Transexudative <30g protein; fluid build up causing back up rpressure e.g. HF/myxoedema coma, low oncotic pressure.
- Exudative >30g protein; inflammatory process - pneumonia, mesothelioma/lung ca, RA/RB, empyema, pancreatitis.
- CXR - blunting of costophrenic angle, meniscus/deviation if large, fluid in lung fissures
- Light’s - at least 1 of the criteria - takes into account protein & LDH
- pleural fluid protein:serum protein >0.5
- pleural fluid LDH:serum LDH >0.6
- LDH >2/3 upper limit of serum LDH
Suspected infected pleural effusion - empyema (2) & mx
- purulent/turbid fluid sample
- clear but pH <7.2 (acidotic) and infection suspcted - improving pneumonia but ongoing fever
- chest drain & abx
Random causes of pleural effusion
* Meig’s syndrome
* Boerhaave’s
* Myxoedema
- ovarian tumour
- ruptued oesophagus
- severe hypothyroidism
Sarcoidosis
* Non-caseating granulomatous condition affecting lungs and other organs. Name 3 extra-pumonary manifestations.
* Why are symptoms worse in summer?
* Ix - what would bloods/CXR/HRCT/bronchoscopy show?
* Mx is generally for symptom releif and to slow progression - main treatment
* Indication for steroid therapy (3) (Prednisolone oral)
* Indication for steroid-sparing Immunosuppressive therapy
- Anterior uveitis, erythema nodosum, kidney stones (hypercalcaemia).
- Increased activation of Vitamin D –> increased serum Ca2+ –> hypercalcaemia
- Raised CRP, ESR, ACE, Ca2+.
- Bilateral hilar lymphadenopathy (stage 1), interstitial infiltrates (stage 2/3), diffuse fibrosis (stage 4)
- Non-caseating granulomas.
- Immunosuppression - glucocorticoids
- Pred if symptomatic, hypercalcaemia, or other organ involvement (heart, eyes, neuro)
Acute sarcodiosis
- name, 3 sx and sign on CXR.
Lofgren’s syndrome
- Polyarthritis
- Fever
- Erythema nodosum
- Bilateral hilar lymphadenopathy
Lung cancer
Small cell & non small cell.
- Most common type?
- Most common subtype in non-smokers/smokers?
- Investigations (4)
- Other bloods
- Treatment for SC vs NSCLC
- NSCLC
- Non-smokers: Adenocarcinoma (NSCLC); Smokers - squamous (NSCLC)
- CXR, staging CT, EBUS –> biopsy for histology, PET-CT
- FBC, LFT, Renal function, INR
- Small cell - chemo.
- NSCLC lobectomy/pneumonectomy.
Small cell lung cancer
* Types of tumour cells
* Associated with which 4 pareneoplastic syndromes…
* Associated with which neurological manifestation
* central/peripheral
* prognosis
- neurosecretory granules –> hormone secretion
- Trosseu’s (mig. thrombo - pro-coagulant factors), Cushing’s (ectopic ACTH), SIADH (ectopic ADH), carcinoid syndrome (ectopic 5HT) and Lambert-Eaten myasthenia gravis
- Limbic encephalitis
- central
- bad - most patients present with advanced disease; cancer is rapidly progressing
Small cell- causes most of pareoneoplastic syndromes - small cell, gives off small molecules
trousseas most common in pancreatic cancer
Adenocarcinoma (NSCLC)
* central/peripheral
* most common type of NSCLC and in ___
*
- peripheral
- non-smokers
note - often normal bronchoscopy due to peripheral location
Squamous cell carcinoma (NSCLC)
* central/peripheral
* secretes
* associated with (2)
* findings on general examination
* name of ca in peripheral region
- causes compression of …(2)
- central
- PTH-related protein –> hypercalcaemia
- hypertrophic pulmonary osteoarthropathy and lambert eaten myasthenic syndrome (but more common in small cell)
- finger clubbing
- pancoast tumour
- brachial plexus - affecting either the sympathetic outflow chain - Horner’s (miosis, ptosis and anhidrosis); or C5/T1 - Klumpke’s palsy (arm pain & atrophy)
Squamous cell - pth producing, pancoast tumours (if peripheral),
Large cell lung cancer
* Secretion of ..
* prognosis?
* peripheral/central
- beta-hCG
- poor
- either
only 10% - the “beta” of NSCLCS - secrete beta HCG
Neurological manifestations of lung cancer
Autoantibodies targeted against cancer cells & pre-synaptic NMJ. Causes proximal & intra-ocular weakness & hyporeflexia.
- What is this called?
- What is post-tetanic potentiation?
- Which antibody is involved?
- Which cancer is this linked to?
- Eaton-Lambert myasthenic syndrome
- after prolonged period of muscle contraction tendon reflex response improves
- Anti-Calcium IgG
- Small and squamous cell carcinoma
Neurological manifestations of lung cancer
* Oncology emergency causing compression of large vessel - resulting in facial swelling, SoB & distended chest vains.
* Name of syndrome?
* Describe Pemberton’s sign.
* Emergency mx.
- Superior vena cava syndrome
Results from any condition that causes obstruction to blood flow in the SVC- invasion/compeession, or thrombosis within the SVC - Lifting arms above head –> facial congestion and cyanosis.
-Most common sx is SOB
-Facial and arm swelling
-Chest pain, dysphagua
-Head fullness when bending forward - Urgent CXR/CT, Dexamethasone. Consider IV stenting.
Neurological manifestations of lung cancer
* hallucinations, memory loss & seizures due to inflammation in the brain & associated with anti-Hu antibodies
- Limbic encephalitis (small cell)
Acanthosis nigricans
- Pareneoplastic syndroe
- Hyperpigmentation in skin folds e.g. neck
- associated with lung cancer, gastric cancer and autoimmune (SLE) etc
Obstructive sleep apnoea
* Sx (night & day)
* Assessment (2)
* RFs
* Inv - Bloods (TFT, FBC), Spo2, BP. Referral to whom for special tests (3)
* Management (3)
* Surgical options
* Who should be informed if causing daytime sleepiness?
- daytime somnolence
- Epworth sleepiness scale and multiple sleep latency test - time taken to fall asleep in dark room
- Acromegaly (macroglossia), hypothyroidism (macroglossia), obesity, palate abnormalities, micrognathia, smoking, alcohol, male sex, motor neurone disease, Marfan’s, large tonsils.
- ENT or specialist sleep clinic
- Polysomnography (ECG & EEG) - includes overnight oximetry, TOSCA (O2 and CO2 monitoring).
- Cons- weight loss, alcohol reduction. CPAP for moderate/severe.
- UPPP - soft palate & jaw reconstruction. Tonsillectomy.
- DVLA
ECG findings for PE
S1Q3T3 (large s, large q, inverted t wave)- indication of right heart strain
RBBB and extreme R axis deviation
Right ventricular strain (t wave inversions in inferior and Anteroseptal leads)
Or sinus tachy
Non specific ST segment and T wave changed
Allergic bronchopulmonary aspergillosis (ABPA)
- risk factor population
- cxr findings
- blood findings
- asthma/CF/chronic lung disease
- upper lobe consolidations
- ## igE and eosinophils raised (hypersensitivity)
Distinguish primary cilary dyskenesia from Kartanger’s dyndrome
**PCD **
- Bronchiecstasis
- Sinusitis
- Male infertility
Kartaneger’s
PCD + situs inversus (dextracardia = “quiet heart sounds”)
Idiopathic pulmonary fibrosis
Presentation: progressive/exertional SOB, dry cough
- Signs on examination
- investigations
- imaging required for diagnosis of IPD
- management (3)
- average life expectancy
- bibasal fine end-inspiratory crackles
- clubbing
- Spirometry: restrictive picture, FEV/FVC increased
- TLCO - impaired-
- Imaging: CXR; HCRT (ground glass opacities –> honeyco,bing)
- ANA +ve or RF +ve (in 30% and 10% respective)
- pulm rehab
- some medications - limited evidence
- supp o2 and lung transplant eventually
- 3-4 years
ma
Acute bronchitis
Chest infection, usually viral, presenting with cough, sore-throat, rhinorrhoea +/- fever, wheeze. Typically clinical diagnosis (+/-CRP) with conservative management (analgesia, oral fluids)
- Differentiate between bronchitis and pneumonia (2)
- Which patients would you consider antibiotic therapy (3)
- What CRP value would warrant a prescription immediately rather than delayed?
- Pneumonia findings on examination: dullness to percussion, crepitations, bronchial breathing (less likely with acute bronchitis). Pneumonia: systemic symptoms more common (fever, myalgia)
- Antibiotics (Doxycycline)
If systemically very unwell
Pre-existing comorbidities
CRP of 20-100 (delayed script) or CRP 100 (offer immediately)
Asbestos-related lung disease
- Most common type, present 20-40 yrs post exposure, bilateral calcifications on CXR, benign, no follow-up reqd
- another common finding on CXR, looks like empyeme/haemothorax
- Lower lung fibrosis caused by asbestos exposure; directly related to length of exposure (latent 15-30 yrs); FEV1:FVC >0.7, reduced TLCO, treated conservatively
- Malignant disease of the pleura; note crocidolite most dangerous asbestos source
- Most common form of cancer associated with asbestosis exposure; synergistic with smoking
- Pleural plaques
- Pleural thickening
- Asbestosis
- Mesothelioma
- Lung cancer
Occupational asthma
* most common cause is isocynates - what is this from?
* other causes = soldering flux resin, flour, platinum salts etc
* investigation
* referral
- spray painting and foam moulding
- serial PEFR measurements at work and away from work
- resp specialist
Indications for NIV (BiPAP/CPAP)
- ABG findings in patient with known COPD (e.g. oxygen not helping so far)
- T2RF (hypercapnic and hypoxic) due to…
- Cardiogenic pulmonary oedema unresponsive to..
- weaning from …
- metabolic acidosis, ph 7.35-7.35
- NMD, chest wall deformity or OSA
- CPAP
- tracheal intubation
Acute respiratory distress syndrome
= non-cardiogenic pulmonary oedema
Due to increased permeabilityof alevolar capillaries –> fluid accumulation
Causes (5)
- Presentation: SoB, tachypnoea
- Sign on ausculation:
- Ix - ABG, CXR
- What can be used to confirm the oedema is non-cardiogenic?
- Requires ITU?
- General management
- What position has been shown to improve outcome?
-
-
- Sepsis, pneumonia, major blood transfusion, COVID, cardio-pulmonary bypass, trauma, smoke inhalation, pancreatitis
- Bilateral lung crackles
- Pulmonary artery wedge pressure
- Yes - generally
- Treat underlying cause. O2/ventilation/organ support
- Prone
*
**
Acut
Atelectasis vs pneumothorax vs consolidation
Alveoli- collapse of alveoli
Air pockets trapped in non ventilated also oil
Caused by airway obstruction - mucus plugs, foreign objects and tumours
Reduce risk by post op chest physio,
Atelectatic lung - deflated balloon, decreased volume
Consolidation - water/pus/blood filled balloon, normal volume
Whereas pneumothorax- air within the pleural space
